Answer

Based on the hemogram there is a poorly regenerative mild anemia with mild thrombocytopenia and a mild to moderate neutrophilia without apparent toxicity or left shift. The anemia is compatible with either acute hemorrhage or hemolysis with insufficient time for regeneration, and or anemia of chronic disease (ACD). The lack of spherocytes or agglutination puts hemolysis lower on the list, and the acute history, if accurate, makes ACD less likely. The hypoproteinemia supports acute blood loss. The thrombocytopenia may be due to in vitro clotting, increased destruction, consumption, or lack of production. The neutrophilia is compatible with either stress, steroids, or acute inflammation, infection, tissue necrosis, or immune mediated disease.

The isosthenuria with azotemia supports renal insufficiency or renal failure. A mild hyperamylasemia with moderate hyperlipasemia suggest decreased renal metabolism, steroid induction, and or pancreatitis. The increased alkaline phosphatase may be due to intra- or extrahepatic cholestasis, or drug induction, especially exogenous or endogenous hypercortisolemia. The increased bilirubin is consistent with prehepatic causes (hemolysis or hemorrhage), or intrahepatic, or posthepatic cholestasis. The mildly increased ALT suggests hepatocellular leakage or drug induction.

Initial rule outs included acute pancreatitis with ascending cholangiohepatitis and renal insufficiency, ethylene glycol toxicity, immune mediated hemolytic anemia, portosystemic shunt, infectious canine hepatitis, toxins, septicemia, lymphoproliferative disease, leptospirosis and immune mediated disease.

Further work-up of this patient involved complete urinalysis, electrolytes, bile acids, ACT, PT, PTT, abdominocentesis, liver fine needle aspiration and hepatic biopsy. Urine bilirubin and blood were markedly increased, and there were fine granular casts stained with bilirubin. The dog was hyponatremic, hypochloremic and hypokalemic, likely as a result of losses from vomiting, renal loss and third space effusions. Bile acids pre- and post- were markedly increased (233, & 299 umol/L respectively), indicating decreased functional hepatic mass. The ACT was slightly prolonged, but the PT and PTT were within normal. DIC was suspected. Abdominocentesis revealed a non-septic modified transudate. Cytology and histology of the liver were in agreement as single cell necrosis, regeneration, intracellular and canalicular cholestasis and mild mixed non-septic hepatitis were reported. Serum titres for Leptospirosis were negative, and PCR was not available at the time. However, one week later the dog had seroconverted with subsequent titres of 1:400 and 1:800 to L. pomona and L. grippotyphosa, respectively.

The dog was treated aggressively with intravenous fluid support and antibiotics (ampicillin and then doxycycline to reduce the carrier state), and she made a full recovery. Treatment with osmotic diuretics, dopamine or loop diuretics such as furosemide is instituted in cases with persistent oliguria or anuria. Penicillin and its derivatives are the antibiotics of choice for elimination of leptospiremia but they do not eliminate the carrier state. Aminoglycosides should be avoided in all cases with renal impairment. Serology using the microscopic agglutination test (MAT) may be negative in acute cases before the dogs have seroconverted (usually around 7-10 days post-infection), but convalescent samples will usually have significant titres. Urine polymerase chain reaction (PCR) may detect cases in the early post-infection stage. More recent subunit vaccines provide protection against 4 or 5 Leptospira serovars while providing protection against infection and urinary shedding after experimental challenge.